Pathogenesis and prevention of necrotizing enterocolitis.

Centre for Reviews and Dissemination, Hull York Medical School, University of York, Heslington, York, UK.
Current Opinion in Infectious Diseases (Impact Factor: 5.03). 03/2011; 24(3):183-9. DOI: 10.1097/QCO.0b013e328345d5b5
Source: PubMed

ABSTRACT Necrotizing enterocolitis (NEC) remains the most common serious acquired gastrointestinal disorder affecting preterm infants. Here we review recent advances in our understanding of the pathogenesis of this multifactorial condition and consider the implications for practice and research.
NEC is an important cause of mortality and serious morbidity in preterm infants. The risk is inversely proportional to gestational age and weight at birth. Fetal growth restriction and compromise may be additional specific risk factors. NEC, particularly severe NEC requiring surgical intervention and NEC with invasive infection, is associated with acute morbidity and mortality and adverse neurodevelopmental outcomes. The principal modifiable postnatal risk factors for NEC in preterm infants relate to enteral feeding practices including formula milk feeding, early and rapid advancement of enteral feed volumes, and exposure to H2-receptor antagonists.
Our understanding of the pathogenesis of this condition remains incomplete. With the exception of feeding with human milk, only limited evidence is currently available to support interventions to prevent NEC. Promising strategies that merit further evaluation in randomized controlled trials include the use of prebiotics and probiotics and the avoidance of exposure to H2-receptor antagonists.

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    ABSTRACT: This report describes the spontaneous intracardiac air contrast found on the echocardiogram of a 5 day-old term neonate with Down syndrome and a complete atrioventricular septal defect who had experienced sudden-onset tachypnea and systemic desaturation. The stream of air contrast was tracked coming from the hepatic veins, and a diagnosis of necrotizing enterocolitis was suspected. An abdominal radiograph and ultrasound confirmed the diagnosis.
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    ABSTRACT: Objective Endogenous digoxin-like factor (EDLF) has been linked to vasoconstriction, altered membrane transport, and apoptosis. Our objective was to determine whether increased EDLF in the cord sera of preterm infants was associated with an increased incidence of necrotizing enterocolitis (NEC). Study Design Cord sera from pregnant women enrolled in a randomized trial of MgSO4 for fetal neuroprotection were analyzed for EDLF using a red cell Rb+ uptake assay in which the inhibition of sodium pump-mediated Rb+ transport was used as a functional assay of EDLF. Specimens were assayed blinded to neonatal outcome. Cases (NEC, n = 25) and controls (neonates not developing stage 2 or 3 NEC, n = 24) were matched by study center and gestational age. None of the women had preeclampsia. Cases and controls were compared using the Wilcoxon test for continuous and the Fisher exact test for categorical variables. A conditional logistic regression analysis was used to assess the odds of case vs control by EDLF level. Results Cases and controls were not significantly different for gestational age, race, maternal steroid use, premature rupture of membranes, or MgSO4 treatment. In logistic models adjusted for treatment group, race, premature rupture of membranes, and gestational age, cord sera EDLF was significantly associated with development of NEC (P = .023). Conclusion These data demonstrated an association between cord sera EDLF and NEC.
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May 24, 2014

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